1. Technical Field
The present invention relates to a method for treatment of emphysema. In particular, the present invention relates to a method for treatment of emphysema by reducing the volume of the pulmonary alveoli or alveolar sacs which have been anomalously expanded with destruction by emphysema.
2. Description of the Related Art
Among a large group of pulmonary diseases that hinder normal respiration is chronic obstruction pulmonary disease (COPD) which brings about lung occlusion on account of at least one disease selected from asthma, emphysema, and chronic bronchitis. COPD frequently involves these diseases at one time and makes it difficult to confirm in each case which one of them really causes the lung occlusion. A case is clinically diagnosed as COPD by constant decrease in expiration flow from the lung over several months, even more than two years for a case of chronic bronchitis. Two of the most critical states relating to COPD are chronic bronchitis and emphysema.
The emphysema denotes a state of anomalous expansion with destruction that occurs in the respiratory bronchioles which permit gas exchange and the tissue called alveolar parenchyma such as pulmonary alveoli, alveolar sac and the like. The alveolar parenchyma in its normal state shrinks at the time of expiration, but the one suffering from emphysema does not recover itself after expansion by respiration. This inhibits normal expiration. Moreover, emphysema decreases the effective area and vascular bed (which denotes capillary vessels running point to point on the surface of the pulmonary alveoli) of the pulmonary alveoli, thereby reducing the gas exchange capacity of the entire lung. In addition, emphysema involves inflammation that destroys elastin and collagen, thereby causing the lung to decrease in elasticity. The result is that the lung cannot keep stretching and expanding the respiratory tract, and this permits the bronchia to deform easily. As the result, the bronchus is compressed to become thin by its surrounding air-filled pulmonary alveoli as the lung shrinks at the time of expiration. This makes the lung expand excessively, preventing air from being discharged easily (see WO 2009/075106 A1, ST MARIANNA UNIVERSITY SCHOOL, MIYAZAWA TERUOMI, “STENT FOR TRATING CHRONIC OBSTRUCTIVE PULMONARY DISEASE”). For this reason, a patient of emphysema purses up his lips to expire (see Jadranka Spahija et al., “Effects of Imposed Pursed-Lips Breathing on Respiratory Mechanics and Dyspanea at Rest and During Exercise in COPD”, Chest 2005; 128:640-650).
In Japan, there are about 50,000 patients with emphysema who are receiving home oxygen therapy, and it is estimated that about three million people including those of mild case are liable to emphysema. At present, the major method of therapy for emphysema is home oxygen therapy. Oxygen therapy is commonly used for the patient who cannot take in sufficient oxygen from air on account of his seriously damaged lung function. However, it merely relieves the patient's condition but it is not an effective method of therapy. On the other hand, there are several methods of pharmacotherapy including: administration of bronchodilator to open respiratory tracts in the lung, thereby alleviating breathing difficulties; administration of steroid by inhalation or mouth, thereby alleviating inflammation in respiratory tracts; administration of antibiotics to prevent or treat secondary infection; and administration of expectorant to remove mucus from respiratory tracts (see Jan A. van Noord et al., “Effects of Tiotropium With and Without Formoterol or Airflow Obstruction and Resting Hyperinflation in Patients With COPD”, Chest 2006; 129:509-517). All of these pharmacotherapies help control emphysema and alleviate its symptom, but they are not necessarily effective. In addition, there are several methods of surgical treatment which include lung reductive surgery which removes damaged parts from the lung, thereby allowing the normal parts of the lung to expand and lung transplantation. However, these methods impose a heavy burden on patients and involved difficulties in securing the lung to be substituted (see Ware J H, et al., “Cost effectiveness of Lung-Volume-Reduction Surgery for Patients with Severe Emphysema”, The New England Journal of Medicine 2003; 348:2092-2102; National Emphysema Treatment Trial Research Group, “A Randomized Trial Comparing Lung-Volume-Reduction Surgery with Medical Therapy for Severe Emphysema”, The New England Journal of Medicine 2003; 348:2059-2073).
If it is possible to carry out “LVR (Lung Volume Reduction)” noninvasively without thoracotomy, many patients will have the chance of therapy. However, the current noninvasive therapy has a low success rate. For example, one of the noninvasive therapy which is expected to produce the same effect as “LVRS (Lung Volume Reduction Surgery)” is an indwelling device in which a one-way valve that prevents the entry of inspired gas into the lung end is left in the bronchus (see Alferness, Clifton A et al., Spiration, Inc., U.S. Pat. No. 6,258,100 B1). However, once left in the lung, it prevents access to any place beyond its indwelling point (see Mark L. Mathis, PneumRx, Inc., U.S. Pat. No. 7,549,984 B1).
It is known that there exists a passage for air flow called bypass, which is different from the main respiratory tract, in the damaged respiratory bronchioles and alveolar parenchyma. Therefore, even through the above-mentioned device prevents air from flowing through the main respiratory tract by the device, air gets around the obstruction by the device to reach the damaged respiratory bronchioles and alveolar parenchyma. Consequently, the above-mentioned device cannot prevent the expansion of the lung (see ALJURI NIKOLAI at al., PULMONX, US 2006/0264772 A1).
There is provided, as another non-surgical method of reducing the lung volume, a method which comprises collapsing a region of the lung and bonding a part of the collapsed region to another region of the lung and further promoting the growth of fiber in the bonded tissue or the vicinity thereof to realize LVR (see Edward P. Ingenito et al., Bistech, Inc., U.S. Pat. No. 6,682,520 B1). In this method, however, it needs a certain length of time for the lung parenchyma to be destroyed by the reaction of the living body. The U.S. Pat. No. 6,682,520 B1 further mentions a method for carrying out LVR by means of a material containing that part of the damaged lung tissue to which targeting therapy is applied. This method needs the part for targeting therapy and also needs a process in which the material reacts with the damaged part (see Gong; Glen et al., PneumRx, Inc., U.S. Pat. No. 7,678,767 B1).
The foregoing suggests that there exists no effective method for treatment of emphysema at present, in the relevant field of art.